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Having a good tooth is essential to health, after all, good teeth can be eaten! But the reality is that about 90% of people in the world have tooth decay, and nearly 2.
4 billion people have tooth decay that has not been treated.
What is tooth decay? When we eat more sweets and carbonated beverages and brush our teeth incorrectly, our tooth enamel will be corroded by cariogenic bacteria and fermented acid to produce rotten and hollow pits.
At this time, our teeth will become very sensitive.
, Blowing cold wind will produce a short-term and strong inflammatory neuralgia, which seriously affects people's appetite and health.
What is even more regrettable is that the mechanism of this cold sensation is still unclear.
Recently, researchers from the University of Erlangen-Nuremberg in Germany and the Howard Hughes Medical Institute (HHMI) in the United States published a study titled Odontoblast TRPC5 channels signal cold pain in teeth in "Science Advances" and their findings The odontoblasts of teeth contain cold sensitive protein TRPC5, which can sense cold and stimulate nerves to transmit pain to the brain.
DOI: 10.
1126/sciadv.
abf5567 previous studies found that in the skin, the two proteins TRPM8 and TRPA1 are key sensors for environmental cold stimuli, and they are also present in high density in the sensory axons of the trigeminal ganglion and dental pulp.
There is also a protein TRPC5 distributed in small and medium-sized trigeminal nerve and dorsal root ganglion neurons, which also exhibits temperature sensitivity and pain sensor functions in heterologous expression systems.
Based on this, researchers speculate that these three proteins may also play a key role in mediating tooth cold stimulation.
In order to study the key cold-conducting ion channel protein of inflammatory tooth pain, the researchers respectively constructed model mice with lack of TRPC5, TRPA1 and TRPM8 and dental pulp injury (DPI).
The pain caused by DPI is manifested as an abnormal increase in sucrose consumption.
The anti-inflammatory and analgesic treatment can eliminate the abnormal intake of sucrose caused by DPI, so the researchers observed the intake of normal temperature sucrose water in each mouse.
The results showed that in TRPA1 and TRPM8-deficient mice, DPI induced a significant increase in sucrose consumption, while the sucrose intake of TRPC5-deficient mice was similar to that of mice without DPI injury.
This indicates that the absence of TRPC5 played a role in eliminating inflammatory pain.
After TRPC5 is essential for inflammatory tooth pain, the function of TRPC5 in mediating cold stimulation pain was further verified by the potential changes of the submandibular alveolar nerve in mice exposed to cold.
At the same time, the researchers found that when using TRPC5 to block When treating mice with agents HC-070 and ML204, they can effectively eliminate the cold stimulus response of certain tooth pain, and reduce the cold response by 59±13% on average.
Among other ion channel proteins that can conduct painful stimuli that have not been blocked, the treatment of TRPA1 blocker HC-030031 has successfully eliminated the residual cold stimulus response mediated by it, with an elimination rate of about 97%, indicating that TRPC5 And TRPA1 is essential for the pain of cold stimulation of teeth.
TRPC5 and TRPA1 are cold sensors in healthy teeth.
How does TRPC5 mediate the cold stimulation pain of normal teeth or pulp-related dental caries and inflammatory diseases? The researchers checked the expression and location of the protein in teeth and found that it was enriched in almost all odontoblasts adjacent to the pulp, and the expression level was higher in pulpitised teeth.
Odontoblasts are a specific cell type located between the dental pulp and dentin, which are connected with nerve axons and other cells of the dental pulp, and can extend to the enamel through the dentin tubules.
The TRPC5 channel is located in the odontoblast cell layer.
After further study, the researchers confirmed the transmission mechanism of tooth cold stimulus pain.
That is, in a cold environment, the cold sensor TRPC5 on the surface of the dentin cell membrane makes the ion channel open to transmit the cold stimulus.
Activate the corresponding nerve, and then the cold stimulation pain is transmitted to the brain through the root nerve, resulting in obvious cold pain.
When teeth are inflamed due to pits due to corrosion, the expression of TRPC5 increases, and odontoblasts become more sensitive to cold, and the electrical signals sent from the root nerves to the brain increase, making pain easier to perceive.
The author of the study, Katharina Zimmermann, said: “Tooth pain may not be considered a popular disease.
This kind of keen sensation has not been studied as extensively as in other scientific fields, but it is very important.
If a more specific target can be developed The sensor drug may eliminate the sensitivity of teeth to cold stimulation, which will affect many people.
"End Reference: [1]https://advances.
sciencemag.
org/content/7/13/eabf5567[2] https://medicalxpress.
com/news/2021-03-teeth-cold.
html
4 billion people have tooth decay that has not been treated.
What is tooth decay? When we eat more sweets and carbonated beverages and brush our teeth incorrectly, our tooth enamel will be corroded by cariogenic bacteria and fermented acid to produce rotten and hollow pits.
At this time, our teeth will become very sensitive.
, Blowing cold wind will produce a short-term and strong inflammatory neuralgia, which seriously affects people's appetite and health.
What is even more regrettable is that the mechanism of this cold sensation is still unclear.
Recently, researchers from the University of Erlangen-Nuremberg in Germany and the Howard Hughes Medical Institute (HHMI) in the United States published a study titled Odontoblast TRPC5 channels signal cold pain in teeth in "Science Advances" and their findings The odontoblasts of teeth contain cold sensitive protein TRPC5, which can sense cold and stimulate nerves to transmit pain to the brain.
DOI: 10.
1126/sciadv.
abf5567 previous studies found that in the skin, the two proteins TRPM8 and TRPA1 are key sensors for environmental cold stimuli, and they are also present in high density in the sensory axons of the trigeminal ganglion and dental pulp.
There is also a protein TRPC5 distributed in small and medium-sized trigeminal nerve and dorsal root ganglion neurons, which also exhibits temperature sensitivity and pain sensor functions in heterologous expression systems.
Based on this, researchers speculate that these three proteins may also play a key role in mediating tooth cold stimulation.
In order to study the key cold-conducting ion channel protein of inflammatory tooth pain, the researchers respectively constructed model mice with lack of TRPC5, TRPA1 and TRPM8 and dental pulp injury (DPI).
The pain caused by DPI is manifested as an abnormal increase in sucrose consumption.
The anti-inflammatory and analgesic treatment can eliminate the abnormal intake of sucrose caused by DPI, so the researchers observed the intake of normal temperature sucrose water in each mouse.
The results showed that in TRPA1 and TRPM8-deficient mice, DPI induced a significant increase in sucrose consumption, while the sucrose intake of TRPC5-deficient mice was similar to that of mice without DPI injury.
This indicates that the absence of TRPC5 played a role in eliminating inflammatory pain.
After TRPC5 is essential for inflammatory tooth pain, the function of TRPC5 in mediating cold stimulation pain was further verified by the potential changes of the submandibular alveolar nerve in mice exposed to cold.
At the same time, the researchers found that when using TRPC5 to block When treating mice with agents HC-070 and ML204, they can effectively eliminate the cold stimulus response of certain tooth pain, and reduce the cold response by 59±13% on average.
Among other ion channel proteins that can conduct painful stimuli that have not been blocked, the treatment of TRPA1 blocker HC-030031 has successfully eliminated the residual cold stimulus response mediated by it, with an elimination rate of about 97%, indicating that TRPC5 And TRPA1 is essential for the pain of cold stimulation of teeth.
TRPC5 and TRPA1 are cold sensors in healthy teeth.
How does TRPC5 mediate the cold stimulation pain of normal teeth or pulp-related dental caries and inflammatory diseases? The researchers checked the expression and location of the protein in teeth and found that it was enriched in almost all odontoblasts adjacent to the pulp, and the expression level was higher in pulpitised teeth.
Odontoblasts are a specific cell type located between the dental pulp and dentin, which are connected with nerve axons and other cells of the dental pulp, and can extend to the enamel through the dentin tubules.
The TRPC5 channel is located in the odontoblast cell layer.
After further study, the researchers confirmed the transmission mechanism of tooth cold stimulus pain.
That is, in a cold environment, the cold sensor TRPC5 on the surface of the dentin cell membrane makes the ion channel open to transmit the cold stimulus.
Activate the corresponding nerve, and then the cold stimulation pain is transmitted to the brain through the root nerve, resulting in obvious cold pain.
When teeth are inflamed due to pits due to corrosion, the expression of TRPC5 increases, and odontoblasts become more sensitive to cold, and the electrical signals sent from the root nerves to the brain increase, making pain easier to perceive.
The author of the study, Katharina Zimmermann, said: “Tooth pain may not be considered a popular disease.
This kind of keen sensation has not been studied as extensively as in other scientific fields, but it is very important.
If a more specific target can be developed The sensor drug may eliminate the sensitivity of teeth to cold stimulation, which will affect many people.
"End Reference: [1]https://advances.
sciencemag.
org/content/7/13/eabf5567[2] https://medicalxpress.
com/news/2021-03-teeth-cold.
html
